Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome of human keratinocytes with or without HPV16 oncogene expression

ABSTRACT: Transcriptome of human keratinocytes with or without HPV16 oncogene expression

PROVIDER: PRJNA511828 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8369874.fastq.gz	Fastqsanger.gz
	SRR8369875.fastq.gz	Fastqsanger.gz
	SRR8369876.fastq.gz	Fastqsanger.gz
	SRR8369877.fastq.gz	Fastqsanger.gz
	SRR8369878.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Transcriptome of human keratinocytes with or without HPV16 oncogene expression

Project description:We used freshly established immortalized human keratinocytes with a well-defined HPV16 E6 E7 expression cassette to get a more complete and less biased overview about global changes induced by HPV16 using RNA-seq. We identified novel factors regulated by HPV oncogenes that could serve an essential role in cancer development.

2019-03-03 | GSE124357 | GEO

Impact of HPV16 E6 and E7 oncogenes together with Chlamydia trachomatis infection on proteome changes in immortalized oral keratinocytes

Project description:Certain types of Human papilloma viruses (HPV) are the etiological agents for cervical cancer. However, not all infections of high-risk HPVs will finally lead to cancer since most HPV infections are cleared without any consequences. Chlamydia trachomatis is the most prevalent sexual transmitted bacteria and is an obligatory intracellular pathogen exhibiting tropism in endocervical epithelial cells. Over the past decades, C. trachomatis is thought to be a potential co-factor for cervical cancer formation, but there are also studies that did not show such a correlation. To address this question in molecular terms, we stably expressed HPV16 E6 and E7 in spontaneously immortalized NOKs (normal oral keratinocytes) and performed SILAC (stable isotope labeling by amino acids in cell culture) with or without C. trachomatis infection to study the impact of HPV16 oncogene expression and C. trachomatis infection on host proteome changes.

2019-03-18 | PXD012186 | Pride

Analysis of gene expression in primary human foreskin keratinocytes (HFK) +/- HPV16 E7

2022-10-31 | GSE208280 | GEO

Analysis of gene expression in primary human foreskin keratinocytes +/- HPV16 E7 or PTPN14 knockout

Project description:This RNA-seq study in primary human forekin keratinocytes was to define genes that are differetially expressed in the presence or absence of HPV16 E7 or several HPV16 E7 variants. We also generated and conducted RNA-seq on primary human foreskin keratinocytes that were CRISPR-Cas9 edited with nontargeting sgRNA or sgRNA targeting PTPN14.

2019-02-28 | GSE121906 | GEO

Human HPV16 positive CaSki cells: Control vs. virus oncogene e6/e7 silenced

Project description:The infection with high-risk human papillomavirus is aetiologically linked to cervical cancer, the role of miRNAs regulated by virus oncogene in cancer progression remain largely unknown. Here, we screened the differentially expressed miRNAs with miRNA array between virus oncogene e6/e7 silenced and not in HPV16-positive cervical cancer cell lines In the study, we screened the differentially expressed miRNAs with miRNA array (Exiqon, miRCURY LNA microRNA array, 7th gen [hsa, miRBase 18]) between virus oncogene e6/e7 silenced and not in HPV16-positive cervical cancer cell lines to found miRNAs regulated by virus oncogene e6/e7. Biological replicates: 3 control, 3 e6/e7 silenced, independently grown and harvested. four replicates per array.

2016-07-01 | E-GEOD-68153 | biostudies-arrayexpress

Human HPV16 positive CaSki cells: Control vs. virus oncogene e6/e7 silenced

2016-07-01 | GSE68153 | GEO

Differentiation resistant HPV16-immortalized keratinocytes: Six1 transfected vs. Control.

Project description:The overexpression of Six1, a member of the Six family of homeodomain transcription factors, has been found in various human cancers, and is associated with tumor progression and metastasis. We previously determined that the expression of Six1 mRNA increased during in vitro progression of human papillomavirus type 16 (HPV16)-immortalized human keratinocytes (HKc/HPV16) toward a differentiation-resistant (HKc/DR) phenotype. However, if Six1 promotes HPV16-mediated transformation or not remains unknown. HKc/DR were transfected with a Six1 or control vector and RNA isolated from these cells were used in an Agilent two-color gene expression profiling experiment. The goal was to determine the effects of Six1 on global gene expression.

2013-12-24 | GSE53589 | GEO

Differentiation resistant HPV16-immortalized keratinocytes: Six1 transfected vs. Control.

2013-12-24 | E-GEOD-53589 | biostudies-arrayexpress

Copy Number Alterations in HNSCC with or without Oncogene Expressing Human Papillomavirus

Project description:Oncogene expressing human papillomavirus type 16 (HPV16) is found in a subset of head and neck squamous cell carcinomas (HNSCC). HPV16 drives carcinogenesis by inactivating p53 and pRb with the viral oncoproteins E6 and E7, reflected by a low level of mutations in TP53 and allelic loss at 3p, 9p and 17p, genetic changes frequently found in HNSCCs of non-viral etiology. We hypothesize that two pathways to HNSCC exist: one determined by HPV16 and one by environmental carcinogens. To define the critical genetic events in these two pathways, we now present a detailed genome analysis of HNSCC with and without HPV16 involvement by employing high resolution micro-array comparative genomic hybridization. Four regions showed alterations in HPV-negative tumors that were absent in HPV-positive tumors: losses at 3p11.2-26.3, 5q11.2-35.2, 9p21.1-24, and gains/amplifications at 11q12.1-13.4. Also, HPV16-negative tumors demonstrated loss at 18q12.1-23, in contrast to gain in HPV16-positive tumors. Seven regions were altered at high frequency (>33%) in both groups: gains at 3q22.2-qter, 5p15.2-pter, 8p11.2-qter, 9q22-34.1, 20p-20q and losses at 11q14.1-qter and 13q11-33. These data show that HNSCC arising by environmental carcinogens are characterized by genetic alterations that differ from those observed in HPV16-induced HNSCC, and most likely occur early in carcinogenesis. A number of genetic changes are shared in both tumor groups and can be considered crucial in the later stages of HNSCC progression.

2009-05-26 | GSE11931 | GEO

Gene expression of cervical cells and immortalized keratinocytes transfected with whole genomes of HPV16 and HPV18

Project description:Human ectocervical and endocervical cells immortalized by HPV16 E6/E7 (designated as Ect and End, respectively) and normal human immortalized keratinocytes (NIKS), were transfected with whole genomes of HPV16 or HPV18, and were subsequently grown in standard monolayer culture until passage 2. Total RNAs were extracted and subjected to TORAY 3D-gene analysis service using the 3D-Gene Human Oligo chip 25K (TORAY, Tokyo, Japan).

2019-08-01 | GSE131076 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data